Influenza A virus (IAV) is one of the most dominant zoonotic-pathogen that causes annually recurring epidemic disease. The detailed molecular mechanism underlying IAV
infection is still not fully understood.
Circular RNAs (
circRNAs) are generated from
RNA back-splicing and involved in diverse biological processes. Here, we employed high-throughput
circRNA microarray technology to profile
circRNA expression in A549 cells in response to IAV
infection. The analysis data revealed that 178
circRNAs expression were significantly upregulated while 137 downregulated, respectively, compared to the mock (P<0.05, Fold Change>2). Subsequently, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were also conducted. Moreover dysregulated
circRNAs were characterized, and of which nine were verified by quantitative real-time PCR (qRT-PCR). We further confirmed that
circRNA_0082633 expression was increased following IAV
infection. Overexpression of
circRNA_0082633 suppressed IAV
infection while depletion of
circRNA_0082633 promoted viral proliferation. Interestingly, the activation of
Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling was involved in IAV-induced circ_0082633 expression. More importantly, we demonstrated that circ_0082633 expression enhanced
type I interferon (IFN) signaling by IFN-stimulated response element (ISRE) promoter activity and Ifnb1
mRNA levels. These data firstly provided the expression profile of
circRNAs in PR8-infected A549 cells and shed new light on the pathogenesis research of IAV
infection. Our findings also suggest that
circRNA_0082633 served an important function in IAV
infection.